PubMed · 13102561
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M J HOGAN. 1952. Atopic keratoconjunctivitis.. https://pubmed.ncbi.nlm.nih.gov/13102561/
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Rhinoconjunctivitis can be caused by allergenic as well as non-allergenic factors. When no allergy is involved, it is important to ask the patient about possible daily exposure to factors that may irritate the mucous membranes. The work environment may play a part, but other things may also be provoking factors, including paper tissues, which, besides the fibres of the paper itself, may contain chemical substances that irritate the mucous membranes. The treatment is to replace the paper tissues with well-washed cotton handkerchiefs. The use of a nasal steroid may be necessary for a short time.
PURPOSE OF REVIEW: To evaluate the pharmacology of current drug development directed towards ocular allergy. Increased worldwide prevalence of ocular allergy has stimulated expansion of management strategies towards physiologic and immunologic drug targets. RECENT FINDINGS: Present drug targets are located in the conjunctival mucosal surface at the initial site of allergen exposure. Pharmacologic intervention attends to early and late phase reactions. Targets generating a response include mast cells, IgE, released preformed mediator histamine, and newly formed mediators, such as prostaglandins, leukotrienes and cytokines. Methods to simulate allergy and measure efficacy of drugs are the conjunctival allergen challenge and the conjunctival provocation test. Pharmacologic outcome is measured via cytologic biomarkers and clinical signs/symptoms of redness, itching, lid swelling and chemosis. Endpoint instruments such as the Ocular Allergy Index and Eye Allergy Patient Impact Questionnaire have emerged from the field of pharmacoeconomics. SUMMARY: Important pharmacologic properties of targets have been revealed. First, histamine is more specifically antagonized by second generation antihistamines. Second, newly formed mediators and downstream responders (prostaglandins, leukotrienes, interleukins, intercellular adhesion molecule 1, tumor necrosis factor, vascular cell adhesion molecule, eosinophils and neutrophils) are more selectively antagonized by dual/multiple-action agents.
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